The lessons science and pharmacology teach us about
achieving optimal health, vitality and maximal lifespan with a low net carb, high saturated fat, evolutionarily paleolithic-styled diet aligned with my ancestral heritage and how I lost 50 pounds of body fat. A sorta fairy story.

Sunday, July 19, 2009

How Crossfit diet and health principles are aligned with TYP... The Paleo diet which 80-90% of all members and trainers follow for optimal performance, gains and superior health... Robb and Nicki's gym (ranked top 30 in the U.S. By Men's Health)... the HAWWT people at my gym... my first warrior trainer Luca who could rip your head off if he wanted to... the MLF who keep us safe (military, law enforcement, firefighters)... how T-Muscle (formerly known as T-Nation) tries to knock it but can't like HERE...

Or the raunchy, hilarious inside jokes about our workouts!

So here is my progress (in my tri Zoot suit)...

Finally my insulin is better controlled (no more tooth abscess b/c it was pulled and the synthetic progestin nearly out of my f*&#$(@ system) after a year of Hormone H*LL... and the 6-paks are re-emerging...again...

Insulin.

It can be your friend or your enemy. It can grow great hypertrophic muscles or screw your metabolism, jack your hsCRP and prevent loss of belly fat.

In my experience (and Robb Wolf's), Paleo and Crossfit control autoimmune diseases and chronic inflammation, the crux of today's modern illnesses including heart disease. Our gym has a story of normalization of NASH/fatty liver disease within ONLY 1 month of Crossfit/Paleo, in addition to stories of complete reversal of IBS cases and many fantastic stories of 30-50 lb-weight loss. Robb has a tale of two pharmacists *cough cough* with NASH/fatty liver (which is autoimmune) and resolution with Paleo eating and Crossfit (one case the liver tests were so high, he was on a liver transplant list), and numerous other stories including one painful/burning, autoimmune lower extremity vasculitis (who I met at his b-day party) and another lifelong cutaneous tarda.

A "Tabata" is 20 seconds of work followed by 10 seconds of rest. 8 rounds total (4 minutes). Count reps for each round. Your 'score' for each exercise is the lowest number of reps completed in any one round.

My score: DL 43# 11 times; DB PP 15# b/c I suck 6 times; burpee 4

The key of course to Tabata is to pace yourself. Don't blow your WOD on the first one to two successive rounds.

Judicious use of medications can bring about therapeutic outcomes or can have dire consequences. In medicine, it is truly an art form to balance the two, more than a science. Science however can provide a better understanding of what ancient doctors like Hippocrates or others in the last half century have known as wisdom and deep experience showed them.

'Mindless Statinators'

(Thanks Barkeater for that phrase *WINK*) Growing evidence shows that statins have 'differential' effects on people who take them. The lower the insulin resistance, the less the small LDL particles are reduced. In fact, two studies have shown that the most potent statin Crestor/rosuvastatin in fact raises small LDL concentrations when Triglycerides (TG, Trig) are less than 120 mg/dl (see first table, above, Kostapanos MS et al. Clin Ther 2007).

Trigs are low in nearly all low-carb compliant TYP'ers! And definitely 100% of people on low carb PALEO.

Crestor is QUITE potent.

At 40mg daily it is THE most potent statin on the market for sledge-hammering down all the LDL particles (large v. small). Caslake et al (Table 2) found that for normotriglyceridemic individuals LDLIII (small dense) % increased from 15.3% to 21.9% (delta = +6.6% sdLDL%) after 8wks only on the maximum dose Crestor 40mg daily (see below graph with comments, the authors failed to put zero on the x-axis...wtf. So please look at how %-sdLDL increases as the Trigs are less than 88 mg/dl = 1.0 mmol/L and even for a great majority of data points less than 177 mg/dl = 2.0 mmol/L).

What a terrible, counterproduct, ANTI-REGRESSIVE adverse drug effect.

TYP Goal for Regression:small LDL NEAR-ZERO or DOWNWARD TREND

The goal for combatting heart disease and to invoke regression/ reversal/ eradication of plaque is to achieve a lower concentration of small dense LDL. Surprising, regression on EBT is frequently reported even before all TYP goals are met! (Wonderful cases of late -- hillbrow, Lindybill, dcarrns!)

Like dense ignorant people, we want the least amount of density and a transformation to lighter, buoyant, more athero-protective LDL particles.

Statins in fact can hinder EBT regression I strongly believe and examples unfortunately exist (the REGRESSION 10yr-subanalysis is an example of higher cardiac mortality in the statin-arm in a sub-group that exhibited a phenotype/genotype for low triglyerides). When an individual temporarily stops or backs off on the dose, the large LDL re-appear and the concentration of small LDL decrease. The sdLDL may not be exceptionally great compared to sdLDL reductions promoted by low LOW carb, mod-high fat diets or ketotic diets, but they DO IMPROVE noticeably as a result from 'statin holidays'. An example of statin suppression of large LDL suppression is for instance if one had an %-sdLDL=300/300=100% improve to 200/400= 50% after stopping Crestor for 1-2mos (Trigs always stay low when a TYP'er stops their statin because nearly all TYP strategies are insulin sensitizing).

That makes sense, right? You don't have to be a 20-year trained cardiologist or lipidologist to understand this data. If Trigs are less than 120 mg/dl, then small LDL concentrations are going to start growing. The graph actually shows that the lower the Trigs go, the HIGHER THE SMALL DENSE LDL CONCENTRATION BECOMES.

Most individuals with severe coronary disease have ALL small dense LDL particles. In fact 100% concentration of sdLDL is not uncommon at all, at the start of the TYP program.

To reach Dr. Davis' goal of 10% concentration of sdLDL, 90% reduction in %-sdLDL would help to achieve regression. It is not the end all, however. It is demonstrated over and over that perfect lipoproteins (esp LDL=60mg/dl) doesn't guarantee SH*T when it's 100% sdLDL. Regression fails to occur in those who persist in over-statinating when the Trigs are excellent less than 120 mg/dl.

Persistently Elevated sdLDL-Concentrations

The signs and symptoms of over-statinating are subtle. They involve persistly high sdLDL-concentrations that do not decrease with TYP strategies, low carb dieting and even the addition of fats which normally remodel sdLDL into large buoyant beautific particles (omega-3, eggs, coconut oil, krill oil, etc). In fact, sometimes (yikes!) the statin effect appears to lead to HIGHER small LDL particle counts and concentrations. Sadly these individuals (to me... IMHO) have disappointing EBT progressions of 10-25% year after year, despite all their wonderful, hard work, good intentions and optimism... Despite spectacular, dramatic reductions in Lp(a).... Unfortunately the Lp(a) is all dense, all small, all drug-related Lp(a) which may actually be accelerating progressive damage.

Would've been better to not be on a statin at all in the first place? Well, perhaps there is value in the first 1-2 wks of the TYP program, but as you can see from post-CAD patients, insulin sensitivity and Trigs are easily controlled with no starch or ketotic diets within only 6 wks (Hays JH Mayo Clinic Proc 2003).

Six weeks... 42 days. Do you have 42 days?

Those who are statin-less at TYP (Mr. 'H', Mr. 'C', Dr. 'K') on the other hand witnessed large %-sdLDL reductions with each NMR or VAP lipoprotein test, perfect increases in large LDL and magnificent reductions in small LDL (even 'NONE') and consequently report EBT regression (Mr. 'C' and Dr. 'K' are pending, I have no doubt). 'Pretty lipoproteins' do not equal regression... it is howthe pretty lipoproteins are achieved and the downward trends, with the minimization of iatrogenic, inflammatory drug effects.

Reduction in small dense LDL% is a very important goal to not ignore for atherosclerotic disease regression and eradication because small dense LDL reflects the internal inflammatory status.

ALL Statins Increase %-Small Dense LDL If Trigs Are Low

Crestor is not alone.

The other statins are NOT exempt.

Lipitor does it too.

They are certainly in fine company. The off-patent generic statins do it as well.

No Starches/High-Fat Diet Decreases %-sdLDL By 10%

I will review this in more detail later but this VERY short trial excellently demonstrates the efficacy and safety of a ketotic diet in post-CAD-event men and women, in producing dramatic lipoprotein changes in only 6wks. By eliminating starches and restricting fruit and increasing protein and dietary cholesterol and fat, concentrations of small dense LDL reduced from 35% to 25%. These patients were on lipid-lowering medications and the average LDL was 100 mg/dl (not high whopper doses of statins apparently). During the feeding diet, Trigs diminished from 147 mg/dl to only 88 mg/dl.